{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T23:57:59Z","timestamp":1790121479791,"version":"4.0.1"},"reference-count":44,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,1,12]],"date-time":"2016-01-12T00:00:00Z","timestamp":1452556800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004156","name":"Mahidol University","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004156","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>As a bone\u2010derived hormone, fibroblast growth factor\u201023 (FGF\u201023) negatively regulates phosphate and calcium metabolism, while retaining growth\u2010promoting action for mesenchymal cell differentiation. Elevated FGF\u201023 levels, together with hyperparathyroidism, are often observed in chronic kidney disease, which is associated with impaired bone mineralization and enhanced bone resorption. Although overexpression of osteoblast\u2010derived osteoclastogenic cytokines might contribute to this metabolic bone disease, whether FGF\u201023 alone and FGF\u201023 plus parathyroid hormone (PTH) directly modulated the expression of osteoblast\u2010derived osteoclastogenic genes remained elusive. Herein, we demonstrated the direct effects of FGF\u201023 on proliferation and mRNA expression of osteoblast\u2010specific differentiation and osteoclastogenic markers in rat osteoblast\u2010like UMR\u2010106 cells in the presence or absence of PTH. FGF\u201023 was found to suppress UMR\u2010106 cell proliferation, while increasing FGF\u201023 expression, the latter of which suggested the presence of positive feedback regulation of FGF\u201023 expression in osteoblasts. FGF\u201023 also upregulated the mRNA expression of osteoblast differentiation markers (e.g., Runx2, osterix, AJ18, Dlx5, alkaline phosphatase, and osteopontin), osteoclastogenic factors (e.g., MCSF, MCP\u20101, IL\u20106, and TNF\u2010\u03b1), and bone resorption regulators (RANKL and osteoprotegerin). However, combined PTH and FGF\u201023 exposure did not alter the levels of FGF\u201023\u2010induced transcripts, suggesting that both hormones had no additive effect. In conclusion, FGF\u201023 directly suppressed osteoblast proliferation, while inducing osteoclastogenic gene expression in UMR\u2010106 cells, and the FGF\u201023\u2010induced transcripts were not altered by long\u2010standing PTH exposure.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbin.10573","type":"journal-article","created":{"date-parts":[[2015,12,23]],"date-time":"2015-12-23T11:18:50Z","timestamp":1450869530000},"page":"329-340","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Expression of osteoclastogenic factor transcripts in osteoblast\u2010like UMR\u2010106 cells after exposure to FGF\u201023 or FGF\u201023 combined with parathyroid hormone"],"prefix":"10.1002","volume":"40","author":[{"given":"Jarinthorn","family":"Teerapornpuntakit","sequence":"first","affiliation":[{"name":"Center of Calcium and Bone Research (COCAB) Faculty of Science Mahidol University Bangkok Thailand"},{"name":"Microarray Laboratory 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